摘要
氧化应激在糖尿病周围神经病变的发病机制中起到了关键作用.高血糖可引起线粒体电子传递链异常、NADPH氧化酶激活等生成活性氧簇,氧化损伤脂质、DNA、蛋白质,促进多个糖尿病周围神经病变的经典病理途径,诱导神经元和雪旺细胞凋亡,神经组织炎症,导致神经损伤.本文就氧化应激与糖尿病周围神经病变发病机制进行综述,为进一步探讨治疗策略提供线索.
Oxidative stress play a key role in the pathogenesis of diabetic peripheral neuropathy.Reactive oxidative species(ROS), derived from hyperglycemia through abnormal mitochondrial electron chain and NADPH oxidase et al, may damage lipids, DNA, and proteins by oxidation.ROS can also promote other classical mechanisms of diabetic peripheral neuropathy, and further cause apoptosis of neurons and Schwann cells, or inflammation of nerve tissue, and finally lead to nerve injury.The relationship between oxidative stress and mechanisms of diabetic peripheral neuropathy was reviewed in this article, in order to get a clue for more effective treatment strategies.
出处
《中华内分泌代谢杂志》
CAS
CSCD
北大核心
2015年第11期1000-1003,共4页
Chinese Journal of Endocrinology and Metabolism
关键词
糖尿病周围神经病变
氧化应激
活性氧簇
Diabetic peripheral neuropathy
Oxidative stress
Reactive oxidative species